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Review
.2015:2015:981328.
doi: 10.1155/2015/981328. Epub 2015 Oct 7.

Helicobacter pylori and T Helper Cells: Mechanisms of Immune Escape and Tolerance

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Review

Helicobacter pylori and T Helper Cells: Mechanisms of Immune Escape and Tolerance

Tiziana Larussa et al. J Immunol Res.2015.

Abstract

Helicobacter pylori colonizes the gastric mucosa of at least half of the human population, causing a worldwide infection that appears in early childhood and if not treated, it can persist for life. The presence of symptoms and their severity depend on bacterial components, host susceptibility, and environmental factors, which allow H. pylori to switch between commensalism and pathogenicity. H. pylori-driven interactions with the host immune system underlie the persistence of the infection in humans, since the bacterium is able to interfere with the activity of innate and adaptive immune cells, reducing the inflammatory response in its favour. Gastritis due to H. pylori results from a complex interaction between several T cell subsets. In particular, H. pylori is known to induce a T helper (Th)1/Th17 cell response-driven gastritis, whose impaired modulation caused by the bacterium is thought to sustain the ongoing inflammatory condition and the unsuccessful clearing of the infection. In this review we discuss the current findings underlying the mechanisms implemented by H. pylori to alter the T helper lymphocyte proliferation, thus facilitating the development of chronic infections and allowing the survival of the bacterium in the human host.

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Figures

Figure 1
Figure 1
The biased Th1/Th2 cells response. The vacuolating cytotoxin (VacA) and the gamma-glutamyl transpeptidase (GGT) secreted by H. pylori inhibit Th1 cell proliferation by inducing a G1/S cell cycle arrest [–31], while the cytotoxin-associated gene pathogenicity island (cag PAI) promotes Th1 death by the induction of Fas ligand [33]. The committed T naïve cells are unable to differentiate into Th1 line due to the enzyme arginase possessed by H. pylori [32]. H. pylori-induced cyclooxygenase- (COX-) 2 activation, alone and in conjunction with its product prostaglandin (PGE), suppresses Th1 polarization [34, 35, 39]. The H. pylori-induced expression of indoleamine 2,3 dioxygenase (IDO) limits the IFN-γ production by Th1 cells and favours the activation of Th2 cells [36]. Stromal factors suppress the IL-12 production by mucosal dentritic cells (DCs) [37], whose dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) receptor interacts with Lewis antigen expressed by H. pylori thus blocking Th1 cell recruitment [38].
Figure 2
Figure 2
The impaired Th17/Treg balance. The induction of Treg cell differentiation is mediated by the overexpression of B7-H1 due to H. pylori cag PAI [41]. On the other hand, the CagA-induced lowered B7-H2 signaling inhibits Th17 cells development from naïve T CD4+ cells [42]. The higher expression of IDO downregulates IL-17 production [36]. DCs promote Tregs differentiation through higher production of IL-18 [44] as well as by a transforming growth factor- (TGF-)β/IL-10-dependent mechanism, which in turn blocks the Th17 cell proliferation [43]. The efficiency of Treg cells themselves is impaired by the production of IL-1β enhanced by the bacterium [47].
Figure 3
Figure 3
The interplay between H. pylori and the effective T helper lymphocytes. Although Th1 and Th17 pathways are both responsible for promoting inflammatory activities during H. pylori infection, neither Th1 nor Th17 cells are by themselves capable of a spontaneous clearance of the infection. It could be due to an impaired release of cytokines, suggesting that a more pronounced inflammation during the early phase of infection could switch the events towards eradication. Th2 response has been implicated in reducing bacterial load but its protective role is still controversial and deserves further investigation. Treg cells limit local inflammation and tissue damage but at the same time this fact favours a tolerogenic status which leads to a persistent infection. This complex interplay suggests that the conflict between persistent infection and clearance is decided in the early phase of infection.
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